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Results for “Recovery phases”

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PubMed2004

The actions of a charged melatonin receptor ligand, TMEPI, and an irreversible MT2 receptor agonist, BMNEP, on mouse hippocampal evoked potentials in vitro.

We have previously determined that melatonin modulates hippocampal synaptic transmission in a biphasic way: an initial depression was followed by a recovery/amplification phase. Here we describe the influence of two novel melatonin receptor ligands, BMNEP (N-bromoacetyl-2-iodo-5-methoxytryptamine) and TMPEI (N-[2-(2-Trimethylammoniumethyleneoxy-7-methoxy)ethyl]propionamide iodide), on the population spike (PS) and excitatory postsynaptic potentials (EPSP) recorded from mouse hippocampal slices. BMNEP, which specifically alkylates and constitutively activates the MT2 melatonin receptor, mimicked the first phase of melatonin's action by irreversibly depressing both the PS and EPSP. TMPEI, a charged ligand of plasma membrane melatonin receptors, amplified those potentials in a manner similar to the effect of melatonin observed during the second, recovery phase. Melatonin had no influence on the potentials amplified by the action of TMPEI. Our results suggest that the biphasic, receptor-dependent action of melatonin and its analogs modulates the efficiency of the hippocampal glutamergic synapse and is most likely mediated through two different, sequentially occurring mechanisms.

5-Methoxytryptamine↗

PubMed1991

Interleukin-2 and natural killer activity in acute type B hepatitis.

Natural killer (NK) cell activity against K562 cell line, and interleukin-2 (IL-2) activity in supernatants from lectin-activated PBMC cultures from 17 patients with acute hepatitis B in the early phase of illness were studied. These patients showed enhanced NK cytotoxicity and higher levels of IL2 activity as compared with control subjects. There was a positive correlation between cytotoxicity values and levels of IL2 activity. Furthermore, in the recovery phase of illness there was a tendency towards normalization in both parameters. When patients were divided in accordance with markers of HBV replication, HBV-DNA positive patients showed increased NK cell activity and IL2 levels as compared with the control group, whereas in HBV-DNA-negative patients no differences were found. However, no differences were found between patients with HBeAg and patients with anti-HBe. These results suggest that natural cytotoxicity is increased early in the course of acute hepatitis B, while NK cell activity returns to normal later, during convalescence. Enhanced NK cell activity appears to be secondary, at least in part, to increased production of IL2. Natural cytotoxicity may be one mechanism that controls the HBV infection before other cytotoxic mechanisms become fully operative.

Acute Disease↗

PubMed1985

Hemolytic-uremic syndrome: demonstration of abnormalities of platelet reactivity and insensitivity to prostaglandin I2.

Platelet aggregation and thromboxane synthesis and platelet sensitivity to the antiaggregatory action of prostaglandin I2 were studied serially in a subject suffering from adult hemolytic-uremic syndrome. Platelet aggregation in vitro was defective during the acute phase of the disease and recovered during the convalescent phase. Defective aggregation was not associated with a failure of thromboxane synthesis although it was related to an intrinsic platelet defect rather than an inhibitor in the plasma. The platelets were insensitive to prostaglandin I2, even in the recovery phase of the disease. Furthermore, plasma from the patient rendered normal platelets insensitive to prostaglandin I2 and more sensitive to aggregating agents. It is concluded that the platelet abnormality in hemolytic-uremic syndrome is complex and it combines both an intrinsic platelet abnormality and a plasma component.

Acute Disease↗

PubMed2004

Rituximab improves peripheral B cell abnormalities in human systemic lupus erythematosus.

OBJECTIVE: B lymphocyte depletion has recently emerged as a promising approach to the treatment of systemic lupus erythematosus (SLE). As part of a phase I/II dose-ranging trial of rituximab in the treatment of SLE, we evaluated the fate of discrete B cell subsets in the setting of selective depletion by anti-CD20 monoclonal antibody and during the B cell recovery phase. METHODS: B cell depletion and phenotype were examined by flow cytometry of peripheral blood mononuclear cells for CD19, CD20, CD27, IgD, and CD38 expression. Changes in autoreactive B lymphocytes and plasma cells were assessed by determination of serum autoantibody levels (anti-double-stranded DNA and VH4.34) and by direct monitoring of a unique autoreactive B cell population bearing surface antibodies whose heavy chain is encoded by the VH4.34 gene segment. RESULTS: Compared with normal controls, SLE patients displayed several abnormalities in peripheral B cell homeostasis at baseline, including naive lymphopenia, expansion of a CD27-,IgD- (double negative) population, and expansion of circulating plasmablasts. Remarkably, these abnormalities resolved after effective B cell depletion with rituximab and immune reconstitution. The frequency of autoreactive VH4.34 memory B cells also decreased 1 year posttreatment, despite the presence of low levels of residual memory B cells at the point of maximal B cell depletion and persistently elevated serum autoantibody titers in most patients. CONCLUSION: This study is the first to show evidence that in SLE, specific B cell depletion therapy with rituximab dramatically improves abnormalities in B cell homeostasis and tolerance that are characteristic of this disease. The persistence of elevated autoantibody titers may reflect the presence of low levels of residual autoreactive memory B cells and/or long-lived autoreactive plasma cells.

Adult↗

PubMed1989

Regrowth kinetics of cells from different regions of multicellular spheroids of four cell lines.

A basic understanding of the recruitment of quiescent tumor cells into the cell cycle would be an important contribution to tumor biology and therapy. As a first step in pursuing this goal, we have investigated the regrowth kinetics of cells from different regions in multicellular spheroids of rodent and human origin. Cells were isolated from four different depths within the spheroids using a selective dissociation technique. The outer cells were proliferating and resumed growth after replating with a 0-8-hour lag period, similar to cells from exponentially growing monolayers. With increasing depth of origin, the lag periods prior to regrowth increased to 2-3 times the monolayer doubling time; cells from plateau-phase monolayers showed a lag period of 1-1.5 times the doubling period. After resuming growth, all cells of a given cell line grew with the same doubling time and achieved the same confluency level. The inner spheroid cells and cells from plateau-phase monolayers had reduced clonogenic efficiencies. The inner cells were initially 1.5-3 times smaller than the outer cells, but began to increase in volume within 4 hours of replating. The fractions of S-phase cells were greatly decreased with increasing depth of origin in the spheroids; there were long delays prior to S-phase recovery after plating, to a maximum of 1-1.5 times the normal doubling time. These results suggest that those quiescent cells from spheroids and monolayers which are able to reenter the cell cycle are predominantly in the G1-phase. However, quiescent cells from the innermost spheroid region require approximately twice as long to enter normal cell cycle traverse as cells from plateau-phase monolayers. The selective dissociation method can isolate very pure populations of proliferating and quiescent cells in a rapid and nonperturbing manner; this system will be valuable in further characterizing quiescent cells from spheroids.

Animals↗

PubMed1995

Effect of an alkaline shift on induction of the heat shock response in human fibroblasts.

The simultaneous exposure of WI-38 human fibroblasts (HF) to a heat shock (45 degrees C, 30 min) and an alkaline shift (> or = pH 8.0) in the incubation medium increased and extended the expression of heat shock proteins (hsps). Hsp70 was the most prominent inducible hsp synthesized during the recovery phase after the double shock, and the increase in synthesis depended on the degree of alkalinization during the heat shock. The accumulation of inducible hsp70, which was shown by Western blotting to occur in the late part of the recovery period, was more pronounced in the cells exposed to alkaline medium during the heat shock. Northern blotting did not reveal any increase in hsp70 mRNA, although time course studies following the double shock indicated a more prolonged presence of mRNA. Hsp70 gene activation was evaluated by a gel retardation assay using a 32P-labelled DNA oligonucleotide containing the heat shock consensus element (HSE) and a heat shock-induced specific binding protein (heat shock transcription factor, HSTF) from the cell extract. Heat shock activated HSTF-DNA binding and induced hsp70 mRNA expression as well as the synthesis and accumulation of hsp70. Alkaline shift, which by itself did not induce hsps expression, activated HSTF DNA-binding. However, in combination with heat shock, alkaline shift enhanced and prolonged HSTF-HSE complex association and hsp expression at both mRNA and protein levels. Since the alkaline shift-induced activation of hsp gene does not allow full transcription, these results provide further support for the multistep nature of the heat shock transcriptional response.

Base Sequence↗

PubMed1982

Determination of related compounds in aspirin by liquid chromatography.

A rapid liquid chromatographic procedure has been validated for the determination of salicylic acid, salsalate, acetylsalicylsalicylic acid, and acetylsalicylic anhydride in aspirin. Samples are dissolved in methylene chloride and analyzed directly by adsorption chromatography in a 7-min separation using an isocratic mobile phase. Recoveries averaged 99% over a 200-10,000 ppm concentration range with standard deviations of less than 4% for the four compounds of interest. Detection limits ranged from 5 to 36 ppm. Compared to a recently published reversed-phase liquid chromatographic procedure for analyzing aspirin, this method is twice as fast, more sensitive, and avoids the use of hydroxylic solvents which lead to degradation of aspirin and acetylsalicylic anhydride.

Aspirin↗

PubMedDate not supplied

Synaptophysin immunohistochemistry during vestibular hair cell recovery after gentamicin treatment.

In the present study, morphometric and immunohistochemical techniques were used to evaluate the degree of synaptic recovery in the chinchilla crista sensory epithelia during various post-gentamicin-treatment periods of hair cell loss and recovery. For this purpose, two groups of animals were treated with Gelfoam pellets impregnated with 50 micro g of gentamicin implanted in the perilymphatic space within the otic capsule of the superior semicircular canal. Animals were sacrificed 1, 2 and 4 weeks after treatment. The degree of synaptic reinnervation was evaluated in the horizontal crista of the first group of animals using immunohistochemical techniques and antibodies against synaptophysin, a marker for synaptic reinnervation and synaptogenesis. Quantification of immunoreactivity in this group was made in the mid-region of the crista using the NIH 'Image' program. The second group of animals was used for quantification of the number of hair cells and supporting cells in the horizontal crista. In the normal sensory epithelium, synaptophysin immunoreactivity was found in the areas corresponding to the known distribution of afferent and efferent nerve terminals. Immunoreactivity was predominantly located within the afferent calyces of type I hair cells. No immunoreactivity was found in the supporting cells. Seven days after treatment there was a significant loss of hair cells and synaptophysin-stained area (SSA). In the mid-region of the crista the loss of synaptophysin immunoreactivity was quantitatively the greatest within the central zone of this region (93%) while the loss of hair cells was the smallest. These results suggest that afferent and efferent nerve terminals were also severely affected by the ototoxic treatment. Four weeks after treatment corresponding to the end of the recovery phase of gentamicin ototoxicity, there was a proportional increase in the number of hair cells and of the degree of SSA in the mid-region of the crista. The number of hair cells recovered to 58% with a recovery of SSA to 54% of normal. These results suggest that a greater fraction of synaptophysin expression within the sensory epithelium depends on the presence of afferent calyceal endings, which are greatly affected by gentamicin. Also, these results demonstrate a significant level of reinnervation of the newly regenerated hair cells, forecasting the potential for functionality of the regenerated hair cells.

Animals↗

PubMed1999

A paucity of unusual trihydroxy bile acids in the urine of patients with severe liver diseases.

To clarify the relationship between the occurrence of unusual trihydroxy bile acids, namely hyocholic acid, ursocholic acid (UCA), and omega-muricholic acid (omega-MCA) in urine and liver disease severity, urinary bile acids were analyzed by gas-liquid chromatography in acute and late phases of acute hepatitis and before and after ursodeoxycholic acid (UDCA) loading in healthy adults and liver cirrhosis patients. In 11 patients with acute hepatitis, the occurrence rates and amounts of unusual trihydroxy bile acids were increased in the late (recovery) phase, as compared with those in the early phase. In 10 patients with severe acute hepatitis who had prothrombin times exceeding 16 seconds, these bile acids had completely disappeared from the urine in the early phase but reappeared in the late phase in those who had a good outcome, though never in a patient who died. After UDCA administration for a week, the amounts of unusual bile acids, especially UCA and omega-MCA, which are thought to be synthesized through 12 alpha- and 6 alpha-hydroxylations, respectively, from UDCA, were clearly increased in 10 healthy adults but only slightly changed in 10 patients with liver cirrhosis. In conclusion, hepatic hydroxylations of dihydroxy bile acids as a detoxification reaction were impaired in severe liver diseases, which may play a role in the intensification and perpetuation of hepatocellular injuries.

Acute Disease↗

PubMed2006

Recovery from experimental allergic encephalomyelitis is TGF-beta dependent and associated with increases in CD4+LAP+ and CD4+CD25+ T cells.

SJL mice are highly susceptible to proteolipid protein (PLP) 139-151-induced experimental allergic encephalomyelitis (EAE). The disease is characterized by a relapsing-remitting type of paralysis. However, the mechanism by which animals recover from EAE is poorly understood. Here, we investigated the role of regulatory T cells in the recovery from disease. We found that Forkhead box P3-expressing CD4+CD25+ T cells were increased in the blood, draining lymph node and spleen of EAE-recovered SJL mice. These cells were anergic and inhibited proliferation of CD4+CD25- T cells to PLP 139-151 or anti-CD3 antibody stimulation. Depletion of CD4+CD25+ T cells during the recovery phase exacerbated disease, resulted in the expansion of IA(s)/PLP 139-151-tetramer-positive cells and enhanced IFN-gamma production. In addition, transforming growth factor-beta (TGF-beta) was shown to be involved in the recovery from EAE as the percentage of CD4+ cells expressing TGF-beta latency-associated peptide (LAP) on the cell surface increased significantly in blood and spleen of EAE-recovered mice as compared with the naive mice and in vivo neutralization of TGF-beta abolished recovery from disease. Taken together, our results demonstrate that both CD4+CD25+ and CD4+LAP+ regulatory T cells mediate recovery from PLP 139-151-induced EAE in SJL mice in which TGF-beta plays an important role.

Adoptive Transfer↗

PubMedDate not supplied

Effect of angiotensin II on striatal dopamine release in the spontaneous hypertensive rat.

We have previously demonstrated that angiotensin II stimulates the release of dopamine from the normotensive rat striatum via the AT1 receptor. In this study, the effect of angiotensin II-stimulated striatal dopamine release in the spontaneous hypertensive rat was compared to normotensive controls. In the spontaneous hypertensive rat, angiotensin II stimulated dopamine release to 169 +/- 13% (P < 0.05) in the experimental period, with levels remaining high in the recovery phase, 158 +/- 16% (P < 0.05). This effect was not significantly different from the response in normotensive controls, in which angiotensin II stimulated dopamine release to 149 +/- 18% (P < 0.05) in the experimental period, with the effect also persisting through the recovery period, 244 +/- 62% (P < 0.05). Thus, despite reports of increased activity of the brain angiotensin II and dopamine systems in the spontaneous hypertensive rat, there is no evidence of abnormal regulation of the striatonigral dopamine system.

Angiotensin II↗

PubMed1993

Calcium metabolism in acute renal failure due to rhabdomyolysis.

We report a patient with drug and hyperthermia induced rhabdomyolysis who developed acute renal failure. During the oliguric phase of 22 days, there was profound hypocalcemia (lowest ionized calcium of 0.34 mmol/l), associated with appropriately elevated intact PTH levels and high normal 1,25(OH)2D levels. Massive calcification in necrotic muscle occurred during this time. In the recovery phase, hypercalcemia was present lasting 33 days (maximum ionized calcium of 1.99 mmol/L), associated with suppression of PTH secretion, low 1,25(OH)2D3 levels, decreased bone resorption and mobilization of the muscle calcium deposits. This case report illustrates that the changes in serum calcium in rhabdomyolysis-associated acute renal failure are explicable by the deposition or removal of mineral into or from necrotic muscle with the parathyroid and vitamin D changes occurring secondarily.

Acute Kidney Injury↗

PubMed2004

The impact of low-dose busulfan on clonal dynamics in nonhuman primates.

An understanding of the number and contribution of individual pluripotent hematopoietic stem cells (HSCs) to the formation of blood lineages has important clinical implications for gene therapy and stem cell transplantation. We have been able to efficiently mark rhesus macaque long-term repopulating stem and progenitor cells with retroviral vectors, and track their in vivo contributions to hematopoiesis using the linear amplification mediated-polymerase chain reaction (LAM-PCR) technique of insertion site analysis. We assessed the impact of busulfan on contributions of individual retrovirally marked clones to hematopoiesis. There were 2 macaques that received transplants of retrovirally transduced CD34(+) cells 2 years previously that were then treated with 4 mg/kg busulfan. Despite only transient and mild suppression of peripheral blood counts, the numbers of individual stem/progenitor clones contributing to granulocyte production decreased dramatically, by 80% in the first monkey and by 60% in the second monkey. A similar impact was seen on clones contributing to T cells. The clone numbers recovered gradually back toward baseline by 5 months following busulfan in the first monkey and by 3 months in the second monkey, and have remained stable for more than one year in both animals. Tracking of individual clones with insertion-site-specific primers suggested that clones contributing to hematopoiesis prior to busulfan accounted for the majority of this recovery, but that some previously undetected clones began to contribute during this recovery phase. These results indicate that even low-dose busulfan significantly affects stem and progenitor cell dynamics. The clonal diversity of hematopoiesis was significantly decreased after even a single, clinically well-tolerated dose of busulfan, with slow but almost complete recovery over the next several months, suggesting that true long-term repopulating stem cells were not permanently deleted. However, the prolonged period of suppression of many clones suggests that transplanted HSCs may have a marked competitive advantage if they can engraft and proliferate during this time period, and supports the use of this agent in nonmyeloablative regimens

Animals↗

PubMed2005

Regulation of cardiovascular functions during acute blood loss.

Sudden blood loss of moderate degree causes fall in blood pressure, which is compensated to certain extent by baroreceptor mediated rise in heart rate and vasoconstriction. In case of severe haemorrhage fall in blood pressure is accompanied by bradycardia indicating failure of baroreceptor mediated recovery in blood pressure. In such conditions partial recovery in the blood pressure with time is possible due to mechanisms other than baroreflex. Therefore, in the present study the regulation of cardiovascular functions on increasing severity of blood loss in the absence of any therapeutic intervention was examined to elucidate the mechanisms involved in the recovery of blood pressure under such conditions. Two groups of animals were studied: (a) In the first group (n = 10) 20% of the total blood volume loss was induced, (b) In the second group (n = 10) 35% of the total blood volume loss was induced. In both the groups cardiovascular parameters were evaluated for one hour after the induction of haemorrhage to record any recovery due to natural compensatory mechanisms. In both the groups there was a significant fall in mean arterial pressure, cardiac output, stroke volume, right atrial pressure and base deficit. A significant increase in heart rate and total peripheral resistance was produced after 1 min of haemorrhage in 20% blood loss while a fall in total peripheral resistance and no rise in heart rate was produced after 35% blood loss. There was a recovery in cardiac output and mean arterial pressure with time in both the cases of blood loss. While a rise in heart rate and stroke volume was produced in 20% blood loss however an initial increase in stroke volume alone and later rise in heart rate alone was produced during recovery phase in 35% blood loss. These finding suggest that 20% blood loss is compensated by baroreflex while 35% blood loss is not accompanied by tachycardia so mechanisms other than the baroreflex, like increase in the vagal tone, contribute to the initial recovery in blood pressure and cardiac output.

Animals↗

PubMed1998

Reversible expression of tryptases and chymases in the jejunal mast cells of mice infected with Trichinella spiralis.

It is has been established that mouse mast cells (MCs) can reversibly alter their expression of serglycin proteoglycans and the homologous granule chymases that have been designated mouse MC protease (mMCP)-1, mMCP-2, and mMCP-5 in vivo. Nevertheless, it remained to be determined whether these immune cells could modify their expression of other chymases and the granule tryptases mMCP-6 and mMCP-7. As assessed immunohistochemically, we now show that MCs reversibly change their expression of the recently described chymase mMCP-9 and both tryptases as these cells traverse the jejunum during the amplification and regression stages of the reactive MC hyperplasia. In noninfected mice, most jejunal MCs reside in the submucosa and express mMCP-6 and mMCP-7, but not mMCP-9 or the chymase mMCP-2. During the inductive phase of the helminth-induced inflammation, when the jejunal MCs move from the submucosa to the tips of the villus, the MCs briefly express mMCP-9, cease expressing mMCP-6 and mMCP-7, and then express mMCP-2. During the recovery phase of the inflammation, jejunal MCs cease expressing mMCP-2 and then express varied combinations of mMCP-6, mMCP-7, and mMCP-9 as they move from the tips of the villus back toward the submucosa. In other model systems, mMCP-6 elicits neutrophil extravasation, and mMCP-7 regulates fibrin deposition and fibrinogen-mediated signaling events. Thus, the ability of a jejunal MC to reversibly alter its tryptase expression during an inflammatory event has important functional implications.

Animals↗

PubMed1997

No effect of glutamate on metabolic disturbances in hippocampal slices of mature fetal guinea pigs after transient in vitro ischemia.

The involvement of glutamate in the development of cerebral metabolic disturbances in mature fetuses after transient ischemia was studied using a hippocampal slice model. We investigated the effects of exogenously applied glutamate or glutamate antagonists on the recovery of energy metabolism and protein synthesis rate (PSR) in hippocampal slices of mature guinea pigs after in vitro ischemia. The slices were incubated in a thermostatically controlled flow-through chamber and gassed with carbogen (95% O2/5% CO2). In vitro ischemia was induced by transferring the slices to an aglycemic, artificial cerebrospinal fluid (aCSF) equilibrated with 95% N2/5% CO2. In a first set of experiments slices were exposed to 10 mM glutamate during a 20-40 min period of in vitro ischemia. In a second set slices were incubated in aCSF containing MK-801 (100 microM) or kynurenic acid (0.5 mM) 30 min before, during and 2 h after in vitro ischemia. After a 12 h recovery phase, the concentrations of adenylates in the slices were measured by HPLC after extraction with perchloric acid. PSR was calculated from the rate of incorporation of [14C]leucine into tissue proteins. Neither glutamate nor glutamate antagonists had any effect on the postischemic recovery of energy metabolism and PSR when applied during in vitro ischemia. It is therefore concluded that glutamate does not play a major role in the development of metabolic disturbances in hippocampal slices from mature guinea pig fetuses subjected to transient in vitro ischemia.

Adenosine Triphosphate↗

PubMed2006

The venous system is the main determinant of hypotension in patients with vasovagal syncope.

AIMS: In patients with vasovagal syncope (VVS), a neural reflex appears the main determinant of hypotension leading to loss of consciousness; whether hypotension is mainly due to involvement of the arterial system or the venous system remains a debated issue. The aim of the present study was to assess which of these two systems is responsible for the fall in blood pressure (BP) in patients with VVS; to this end, a haemodynamic study was carried out not only before and during loss of consciousness but also during the recovery phase. METHODS AND RESULTS: Beat-to-beat recordings of heart rate (HR), BP (volume-clamp method) and stroke volume (SV) (modelflow method), cardiac output (CO), and total peripheral resistance (TPR) were made at rest, during unmedicated tilt testing (TT) and recovery from loss of consciousness in 18 patients with a history of syncope (age 45+/-23 years) and positive response to TT. Blood pressure showed a significant fall during prodromal symptoms and a further fall at the beginning of loss of consciousness, together with a fall in SV, CO, and HR, and a slight, but significant, increase in TPR. At the beginning of recovery, BP showed a significant increase and a further increase 5 min later, together with an increase in SV, CO, and HR without significant changes in TPR. CONCLUSION: These results suggest that in VVS the fall in BP is mainly caused by reduced venous return to the heart. The arterial system does not appear to be the main determinant of the fall of BP; however, the system appears unable to make the appropriate compensatory changes.

Blood Pressure↗

PubMed1987

Positive effects of indomethacin on restoration of splenic nucleated cell populations in mice given sublethal irradiation.

Splenic cellularity during the recovery phase after 400-R irradiation was evaluated in mice, in which the level of prostaglandin was regulated by indomethacin and exogenous prostaglandin E2, following sublethal irradiation. Two weeks after irradiation, administration to these mice of indomethacin, an inhibitor of prostaglandin synthesis, augmented the recovery of all nucleated spleen cell populations, whereas the thymus was drastically depopulated. This treatment had little effect upon the total number of bone marrow cells but inversed the ratio of PNA+/PNA- cells. Cell transfer experiments using heavily irradiated mice as recipients showed that the stem cell proliferation was positively affected by indomethacin treatment in the bone marrow rather than in the spleen. These results suggest that cell migration from primary lymphoid organs, particularly from the bone marrow to the spleen, is regulated by a prostaglandin-mediated system and that a prostaglandin E2 synthesis inhibition would have a positive effect on the restoration of peripheral nucleated cells following irradiation.

Animals↗